Rostral transfontanel herniation.

Upward transtentorial herniation as a result of mass effect in the posterior fossa has been described in adults by several authors. We report the case of a premature infant, small for gestational age, who experienced rostral herniation of a portion of frontal lobe through the anterior fontanel as the result of a hemorrhagic cerebellar infarction followed by a large parieto-occipital intracerebral hemorrhage.     

Initial enlargement of the opposite pupil as a false localising sign in intraparenchymal frontal haemorrhage.

Ipsilateral third nerve palsy with early pupillary enlargement is an important sign of transtentorial herniation from a supratentorial mass lesion. A case of frontal, intraparenchymal haemorrhage is reported in which the first ocular manifestation of transtentorial herniation was enlargement of the contralateral pupil. The ipsilateral pupil dilated only after complete oculomotor palsy of the contralateral eye. After partial frontal lobectomy and removal of blood clot, the ipsilateral third nerve recovered before the contralateral third nerve. Clinical findings localised the contralateral third nerve lesion to an extra-axial site. The possible mechanisms of contralateral third nerve compression are discussed. This seems to be the first example of pupillary enlargement as a false localising sign from a contralateral, supratentorial, intraparenchymal mass lesion.     

Fatal outcome of ischemic cerebral infarct

During 1977 to 1985 2008 patients suffering from acute ischemic cerebral infarcts were admitted to the Department of Neurology, Giessen University. 213 (10.6%) died during their stay at hospital of 28 days in average. Time of survival, cause of death, localization and etiology of the infarcts were evaluated retrospectively on base of the medical reports, the angiographic, doppler-sonographic, computerized tomographic, and autopsy findings. The same number of patients died because of direct sequelae of stroke and secondary complications respectively. Those with supratentorial infarcts, who died in consequence of a vegetative dysregulation generally did not survive the first week after ictus, often had infarcts exceeding the supply area of one large cerebral artery and frequently had evidence of cardiac embolism. Pathogenetic factors for extension of the ischemic cerebral damage subsequently causing transtentorial herniation were spreading thrombosis, reinfarction, and fatal secondary hemorrhage. Patients dying in consequence of an infratentorial infarct often had a thrombosis of the basilar artery or a large cerebellar infarction. Secondary fatal complications mostly occurred after the first week after stroke. Pulmonary edema, pulmonary embolism and myocardial infarction predominated with different time pattern.     

Syndrome of transtentorial herniation: is vertical displacement necessary?

MRI from a comatose patient with a massive acute subdural haematoma showed most of the features of transtentorial herniation described in the classic pathology literature. In addition to encroachment on the perimesencephalic cisterns, infarction in the anterior and posterior cerebral artery territories, ischaemic change in the lower diencephalon, and ventricular enlargement were visualised. Despite the clinical syndrome and these secondary changes due to compression, there was only approximately 2 mm of downward displacement of the upper brainstem compared with 13 mm horizontal displacement. Although tissue shifts adjacent to the tentorial aperture cause brainstem and vascular compression, these changes may occur with minimal downward herniation.     

Hemicraniectomy in elderly patients with space occupying media infarction: improved survival but poor functional outcome

OBJECTIVE: To assess the survival rate and functional outcome in elderly patients with space occupying supratentorial infarction who underwent hemicraniectomy compared with those who received medical treatment alone. METHODS: All patients older than 55 years with space occupying middle cerebral artery (MCA) infarction treated in our clinic between January 1998 and July 1999 were included in this retrospective analysis. Patients were eligible for decompressive surgery if they were younger than 75 and had no severe comorbidity. Hemicraniectomy was performed regardless of the affected hemisphere. All patients were followed up for assessment of functional outcome; data were assessed according to the Barthel index and modified Rankin scale and cover a period of 3 to 9 months after infarction. RESULTS: Twelve out of 24 patients underwent hemicraniectomy. Eight patients who were operated on survived; only one patient died of transtentorial herniation, three other deaths were due to medical complications. None of the survivors had a Barthel score above 60 or a Rankin score below 4. Nine out of 12 medically treated patients died of transtentorial herniation, one patient died of medical complications. The two surviving patients had a Barthel score below 60 and a Rankin score of 4. CONCLUSIONS: Craniectomy in elderly patients with space occupying MCA infarction improves survival rates compared with medical treatment alone. However, functional outcome and level of independence are poor. Craniectomy in elderly patients should not be performed unless a prospective randomised trial proves beneficial.     

Paradoxical fixed dilatation of the contralateral pupil as a false-localizing sign in intraparenchymal frontal hemorrhage

Unilateral fixed pupillary dilatation represents an important clinical sign of transtentorial herniation of an ipsilateral mass lesion. Rarely the contralateral pupil is affected to produce a false-localizing sign. Two cases of this paradoxical contralateral fixed pupillary dilatation involving intra-axial lesions have been reported. We report a case of a 33-year-old man with a left frontal intraparenchymal hemorrhage who developed a false localizing fixed dilatation of his right pupil, which resolved after craniotomy and evacuation of the clot. The possible mechanisms of contralateral third nerve palsy are discussed.     

小脑后下动脉解剖变异致双侧小脑梗死2例报道并文献复习

目的 探讨小脑后下动脉(posterior inferior cerebellar artery, PICA)解剖变异致双侧小脑梗死的临床特征及发病机制。方法 对2例经颅脑MRI确诊的双侧小脑梗死患者采用CT血管造影(CTA)、磁共振血管成像(MRA)或数字减影血管造影(DSA)显示其头颈部血管,从而了解后循环血管的形态特征并复习相关文献。结果 病例1经DSA证实左侧椎动脉较细,远端管腔闭塞,通过右椎动脉代偿供血原左侧PICA供血区但欠充分,双侧PICA共同起源于右侧椎动脉。病例2经CTA证实右侧椎动脉较左侧明显细且远端显示欠清,MRA示双侧PICA共同起源于左侧椎动脉。结论 2例双侧小脑梗死患者均存在一侧椎动脉优势供血,且双侧PICA共同起源于该侧椎动脉。在该解剖变异基础上一侧椎动脉发生病变时可出现双侧小脑梗死。因此,在临床中出现双侧小脑梗死时临床医师不能忽略这一解剖变异基础。     

Cerebellar infarction in the territory of the superior cerebellar artery: a clinicopathologic study of 33 cases

We reviewed the clinical and pathologic findings in 33 patients with infarcts in the territory of the superior cerebellar artery (SCA). The clinical manifestations included the rostral basilar artery syndrome (8); coma at onset, often with tetraplegia (11); cerebellar and vestibular signs (9, with delayed coma due to cerebellar swelling in 6); and, in only 1 patient, the "classic" syndrome of the SCA. Clinical features were overshadowed by an infarct in the territory of the middle cerebral artery in 3 other patients, and the diagnosis was made only at autopsy in a fourth. Pathologically, SCA infarcts occurred in isolation in 7 patients. The most striking finding was the high frequency of associated infarcts in the territory of the rostral part of the basilar artery (73%). One-third of patients also had an infarct in the territory of the posterior inferior cerebellar artery, sometimes associated with infarction of the anterior inferior cerebellar artery. Tonsillar herniation was observed in 15 patients, 8 of whom had no infarcts in other cerebellar territories. Occlusions occurred mainly in the distal basilar artery and distal vertebral artery. The infarcts were mostly caused by cardiac and artery-to-artery emboli.     

Diffuse postoperative cerebellar swelling in medulloblastoma: report of two cases

Background  

We report two cases of diffuse cerebellar swelling with upward transtentorial herniation following medulloblastoma resection. We present our insight for managing medulloblastoma with aggressive clinical behavior.     

Paradoxical ventriculomegaly due to low-pressure hydrocephalus,a rare complication of the treatment of a trapped fourth ventricle: Case report

In this paper, we describe the rare phenomena of descending transtentorial herniation and paradoxical ventriculomegaly due to low pressure hydrocephalus. This resulted as a complication of treatment in a 14 year old male patient, who had undergone multiple ventriculo-peritoneal shunt placements for hydrocephalus after resection of pilocytic astrocytoma. We discuss the etiology of this rare complication and our strategy for treatment. We emphasize the need for strategic placement of programmable shunts to avoid over shunting and associated complications such as tentorial herniation.     

Upward transtentorial herniation: seven cases and a literature review.

Seven cases of upward transtentorial herniation occurred. In each patient, coma with reactive, miotic pupils, asymmetrical or absent caloric responses, and decerebrate posture indicated brain-stem compression. In this setting, the development of unequal, then midposition, fixed pupils signaled midbrain failure from upward herniation. Vertebral angiography showed upward displacement of the superior cerebellar arteries. Results of autopsy confirmed the existence of grooving of the vermis by the tentorial margins and, in one case, of anterior displacement and distortion of the midbrain. In five of 45 reported cases of upward herniation, the conditions were diagnosed antemortem. Instances of cerebellar hematoma and tumor predominated. In at least seven patients, performance of ventriculography may have precipitated herniation. Clinical details were provided in only nine patients and did not separate upward herniation from brain-stem compression. Cerebellar ischemic infarct found in one of our patients is a rarely reported cause of upward herniation.     

Cerebellar infarction in the area of the posterior cerebellar artery. Clinicopathology of 28 cases

We report a neuropathological study of cerebellar infarctions involving the territory of the posterior inferior cerebellar artery (PICA) in 28 cases. Fifteen cases involved the PICA territory only. In 13 cases infarctions in the anterior inferior cerebellar artery (AICA) territory and/or in the superior cerebellar artery (SCA) territory were also present. A thorough post-mortem study of the arterial supply of the brain from the heart up to the cerebellar arteries, including the cervical spine segment of the vertebral arteries was performed in 27 cases. The territory of the cerebellar infarcts has been ascertained. In 15/28 cases (54 percent), infarction involved the PICA territory only (17 infarcts). All of these cases had a benign outcome and death was due to another cause. Six of these were recent infarctions. None had evidence of swelling and tonsillar herniation. Infarcts were generally of small size and involved the entire PICA territory in only 2 cases. Most of these cases were unexpected discovered at autopsy. Cerebellar infarction in the territory of the medial branch of the PICA (9/17 infarcts) drew grossly a set square with a dorsal base and a ventral top headed for the IVth ventricle. Five out of these cases were associated with infarction in the dorsal and lateral medullary territories. Retrospective clinical study showed that they had been unnoticed or overshadowed by other neurological disorders (4 cases), or presented as Wallenberg's syndromes (4 cases), or as a pure vestibular syndrome (due to an infarction involving only the cerebellum) mimicking an acute labyrinthine disorder (1 case). Infarctions in the territory of the lateral branch of the PICA (5/17 infarcts) always occurred without medullary involvement. All of them were unexpectedly discovered at autopsy, and were unnoticed during the life (3 infarcts) or were overshadowed by other neurological disorders (2 infarcts). That was also the case in 2 cases of infarction in the whole PICA territory (3/17 infarcts). Thus infarctions strictly localized to the entire PICA territory only were rare. Thirteen/28 cases (46 p. 100) of infarction in the whole PICA territory were associated with infarction in the AICA and/or the SCA territories. This resulted from an association with other infarctions and not from an abnormally large territory of the PICA. Cerebellar swelling with brain stem compression and tonsillar herniation occurred 8/13 cases (62 p. 100). There were other massive median and paramedian brain stem infarctions involving midbrain, pons or medulla in 55 p. 100 of 13 cases.(ABSTRACT TRUNCATED AT 400 WORDS)     

Therapy of severe ischemic stroke: breaking the conventional thinking

Large hemispheric infarcts must be recognized in the emergency department as a life-threatening condition that requires prompt and massive intervention. After stabilization of the airway, breathing, and circulation, the initial diagnostic work-up and transfer to a neurointensive care unit should not be delayed. Today several new therapeutic options can be offered. Surgical decompression seems to be effective in lowering increased intracranial pressure, preventing transtentorial herniation and reducing mortality in patients with malignant middle cerebral artery infarction. Another option may be therapeutic hypothermia, which has been found to be neuroprotective in animal models, as well as in clinical studies after cardiac arrest. Experience in stroke patients suggest that hypothermia may offer a new approach for the treatment of acute cerebral ischemia.     

Cerebellar infarction and internal hydrocephalus

Four cases of acute cerebellar infarction producing hydrocephalus are presented. Only the patient, who is submitted to surgical decompression of the posterior fossa, survives, while the other three die. In the latter the necropsy shows a hemorrhagic cerebellar softening in the territory of the inferior posterior cerebellar artery, causing tonsillar herniation and impairment of the liquor drainage at the level of the inferior part of the 4th ventricle. It is suggested that the infarction and the hydrocephalus further progress in "avalanche effect", which is fatal unless prompt surgical decompression can be carried out.     

Disappearance of resting tremor after thalamic stroke involving the territory of the tuberothalamic artery

Disappearance of resting tremor was observed in a 76-year-old patient with Parkinson's disease after a contralateral thalamic infarct involving the territory of the tuberothalamic artery. Based on the analysis of surgical data of Parkinson's disease patients, this might be explained by the lesion of the ventral lateral nucleus, which is supplied by the inferolateral and tuberothalamic arteries. Thalamic infarction in the territory of the tuberothalamic artery as well as the inferolateral artery can produce amelioration of tremor.     

Transient upper monoballism in the presence of contralateral chronic subdural hematoma

A case of chronic subdural hematoma associated with contralateral upper monoballism is reported. Intracranial midline shift and transtentorial herniation of the ipsilateral temporal lobe were the only demonstrated CT abnormalities. Complete neurological recovery followed the evacuation of the hematoma. Direct mechanical injury caused by the marked brain compression and distortion, and transient ischemic changes within cerebral areas whose damages may result in ballism, may be considered important causative factors of such an unusual neurological complication.     

Crossed cerebellar hypoperfusion in hyperacute ischemic stroke

OBJECTIVE: In chronic stage of cerebral hemispheric infarction, contralateral cerebellar blood flow and metabolism are depressed, which is known as crossed cerebellar diaschisis (CCD). The present study was performed to elucidate (1) whether the diaschisis occurs in hyperacute stage of ischemic stroke when computed tomography (CT) scans is not able to identify infarction, and (2) which site of lesion in the cerebrum is responsible for the depression in contralateral cerebellar blood flow. METHODS: Single photon emission computed tomography was performed in 21 patients with middle cerebral artery (MCA) embolic infarction within 6 h of the onset (3.2+/-1.1 h, mean+/-S.D.). Regions of interest (ROIs) were symmetrically located in the cerebral hemispheres including cerebral cortex and subcortex, and in the cerebellar hemispheres. RESULTS: The side-to-side ratio of cerebellar blood flow ipsilateral to that contralateral to cerebral infarct was significantly increased compared with that in normal control (P<0.001), indicating that contralateral cerebellar blood flow was significantly depressed. In hyperacute stage, the ratio of cerebellar blood flow appeared to be associated with the ratio of cerebral blood flow in whole hemispheres (r=0.44, P<0.05), in anterior frontal lobe (r=0.44, P<0.05) and in anterior temporal lobe (r=0.58, P<0.01), but not in infarct areas (r=0.26, P=0.3). Stepwise regression analysis revealed that the ratios in cerebellar hemispheres were associated with those in anterior temporal lobe (multiple regression analysis, r=0.58, P<0.01). CONCLUSIONS: Crossed cerebellar diaschisis occurs at hyperacute stage of stroke of the MCA infarction. It may be related to the hypoperfusion in the anterior frontal and anterior temporal lobes of the cerebrum where regional blood flow is decreased by ischemic infarction per se or by ipsilateral hemispheric depression from infarct area (diaschisis mechanism).     

An uncommon cause of stroke in young adults.

We describe a previously healthy 48-year-old man who presented with clinical characteristics suggestive of internal carotid artery dissection, confirmed by magnetic resonance imaging. He developed a massive infarction of the left cerebral hemisphere and died after 3 days of transtentorial herniation. Post-mortem examination identified a dissection of the thoracic aorta caused by Erdheim-Gsell cystic medionecrosis, with the characteristic degeneration of the elastic fibers of the lamina media. The dissection showed an unusually large extension not only distally into both iliac arteries, but also proximally into both carotid arteries. To our knowledge, such an extensive dissection has not been described previously. Underlying vessel wall disorders of the aorta, such as Erdheim Gsell cystic medionecrosis, should be considered in young patients with spontaneous arterial dissection.     

小脑梗死的分型与后循环血管病变

目的 研究有无大血管病变患者小脑梗死灶的特征,探讨小脑梗死分型与后循环血管病变的关系。 方法 收集我科自2006年1月～2008年3月期间住院的小脑梗死患者共35例,所有患者均同时具备颅脑磁共振成像（magnetic resonance imaging,MRI）和血管造影检查,包括计算机断层摄影血管造影（computed tomographic angiography,CTA）、磁共振血管造影（magnetic resonance angiography,MRA）和数字减影血管造影（digital subtraction angiography,DSA）检查。根据血管造影检查的结果将入组患者分为两组：大血管病变组20例,小血管病变组15例,分析两组小脑梗死的分型和后循环血管病变（包括狭窄或闭塞）的关系。 结果 ⑴大血管病变组20例中,颅内血管（椎动脉颅内段或基底动脉）病变最多见（10例,50%）,梗死类型多为分水岭梗死（7例,70%）;其次为颅外血管合并颅内血管（椎动脉颅外段合并颅内段或基底动脉）病变（8例,40%）,梗死灶多为小脑后下动脉（PICA）供血区的区域性梗死（7例,87.5%）;单独颅外血管（椎动脉颅外段）病变最少见（2例,10%）,梗死分布无明显倾向性。⑵小血管病变组15例中,梗死灶亦多位于分水岭区（9例,60%）。 结论 由于小脑血液供应特点,小脑梗死中分水岭梗死和腔隙性梗死较区域性梗死更为常见。小梗死灶（直径≤2cm）可能存在后循环大血管的狭窄或闭塞,应予积极的治疗和干预,以防病情加重。     

Fatal or severely disabling cerebral infarction during hospitalization for stroke or transient ischemic attack

Summary Six (1%) of 578 patients admitted for cerebral infarction or transient ischemic attack (TIA) suffered a fatal or severely disabling in-hospital cerebral infarction following a period of stabilization or improvement lasting more than 1 day. These infarctions were characterized by the sudden onset of stupor or coma and subsequent development of transtentorial herniation due to carotid or middle cerebral artery territory infarction, or widespread brain-stem infarction due to basilar occlusion. Only one patient survived. Four patients had largevessel disease documented by Doppler, angiography, or at autopsy. Each of these six infarcts occurred during the morning hours, 4–9 days after the initial event, 3–8 days after initiation of intravenous heparin, and within 4–8 h after intravenous heparin had been discontinued. No coagulation abnormalities were documented. We believe that these cases indicate that among patients admitted for cerebral infarction or TIA, fatal or severely disabling in-hospital cerebral infarction after a period of stabilization or improvement may occur in patients having an initially mild to moderate clinical deficit, that those suffering large artery disease may be at greater risk, and that there may be a relationship between heparin withdrawal and cerebral infarction in some patients.Supported in part by the Sunny von Bulow Coma and Head Trauma Research Foundation